Abstract

The fusion machinery for herpesvirus entry in the host cells involves the interactions of viral glycoproteins with cellular receptors, although additional viral and cellular domains are required. Extensive areas of the plasma membrane surface consist of lipid rafts organized into cholesterol-rich microdomains involved in signal transduction, protein sorting, membrane transport and in many processes of viruses infection. Because of the extraction of cholesterol leads to disorganization of lipid microdomains and to dissociation of proteins bound to the lipid rafts, we investigated the effect of cholesterol depletion by methyl-- cyclodextrin (MCD) on caprine herpesvirus 1 (CpHV.1) in three important phases of virus infection such as binding, entry and post-entry. MCD treatment did not prejudice virus binding to cells, while a dose-dependent reduction of the virus yield was observed at the virus entry stage, and 30 mM MCD reduced infectivity evidently. Treatment of MDBK after virus entry revealed a moderate inhibitory effect suggesting that cholesterol is mainly required during virus entry rather than during the post-entry stage. Alteration of the envelope lipid composition affected virus entry and a noticeable reduction in virus infectivity was detected in the presence of 15 mM MCD. Considering that the recognition of a host cell receptor is a crucial step in the start-up phase of infection, these data are essential for the study of CpHV.1 pathogenesis. To date virus receptors for CpHV.1 have not yet been identified and further investigations are required to state that MCD treatment affects the expression of the viral receptors.

Autore Pugliese

• Pratelli Annamaria

Tutti gli autori

• PRATELLI A.;COLAO V.

Titolo volume/Rivista

Non Disponibile

Anno di pubblicazione

2016

ISSN

0168-1702

ISBN

Non Disponibile

Numero di citazioni Wos

1

Ultimo Aggiornamento Citazioni

Non Disponibile

Numero di citazioni Scopus

1

Ultimo Aggiornamento Citazioni

Non Disponibile

Settori ERC

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Codici ASJC

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